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Immunobiome-POSTECH Research Team Discovers New Drug Candidate Targeting Multiple Sclerosis and Inflammatory Bowel Disease

[Asia Economy Reporter Hyunseok Yoo] Immunobiome, a microbiome-based therapeutic research and development company, and the Department of Life Sciences research team at Pohang University of Science and Technology (POSTECH) announced on the 15th that they have identified that MGCP (Mannan/β-Glucan containing polysaccharides), a polysaccharide mixture extracted from yeast, suppresses the onset and progression of hypersensitive immune diseases such as autoimmune diseases.


MGCP is one of the microbiome-based therapeutic candidate substances secured by Immunobiome. Unlike microbial metabolites and microbe-derived metabolites used in existing microbiome therapeutic development, MGCP identifies the active substances of microbes and selectively controls various inflammatory diseases based on precise mechanisms of action. Due to the nature of microbiome-derived substances, there are almost no side effects, and especially, therapeutic development technology based on these active substances is gaining attention as the next-generation microbiome therapy.


The Immunobiome and POSTECH research teams focused on anti-inflammatory substances derived from microbes that greatly influence immune system development and regulatory functions in this study. They isolated MGCP, a polysaccharide mixture with a specific structure from yeast, one of the human symbiotic microbes, and evaluated its immune regulatory efficacy in vitro and in mice, observing that MGCP suppresses inflammatory immune responses.


In particular, through experimental mouse model studies of inflammatory bowel disease and multiple sclerosis, mice administered with MGCP showed inhibited generation of type 1 helper T cells (hereafter Th1 cells), which promote inflammatory immune responses. Additionally, MGCP induced the generation of regulatory T cells (hereafter Treg cells), which suppress overall immune responses, confirming that it can inhibit the onset and progression of inflammatory diseases.


Dr. Dipayan Rudra of Immunobiome made significant contributions to completing this study. Through joint research with the POSTECH team, they demonstrated that the mechanisms of MGCP-induced immune suppression?namely, the inhibition of Th1 cell generation and induction of Treg cell generation?are mediated by two different innate immune receptors expressed on dendritic cells, TLR2 and Dectin1. They revealed that the previously known immune-enhancing effect of β-glucan is due to β-1,3-glucan, and discovered that β-1,6-glucan, a component of MGCP, has an immune-suppressive effect.


These research results are recognized as groundbreaking, proving that the contradictory functions of beta-glucan?anti-inflammatory or immune-enhancing?are due to structural differences between beta 1-3 and beta 1-6.


Shinhyuk Lim, CEO of Immunobiome and professor at POSTECH’s Department of Life Sciences, stated, "This research result will greatly aid the development of next-generation therapeutics that can overcome the limitations of existing inflammatory immune disease drugs, which have significant side effects." He added, "We will continue additional research to determine whether MGCP effectively acts on other inflammatory immune diseases."


Meanwhile, this research achievement was published online on the 14th at 6 p.m. (Korean time) in the prestigious international journal Nature Communications (IF 12.121).


Inflammatory bowel diseases such as Crohn’s disease and ulcerative colitis, and autoimmune diseases such as multiple sclerosis, are rare inflammatory intractable diseases caused by problems in regulating the human immune system. Their exact causes are unknown, but genetic and environmental factors are presumed to influence their onset. Currently, agents that suppress overall inflammatory responses are used as treatments in clinical settings, but they have significant side effects such as increased susceptibility to infections, and thus, effective treatments have yet to be developed.


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